Search Results (297)

Psychological stress can affect female reproductive function through behavioral, endocrine, ovarian, and oxidative mechanisms. Antioxidant supplements have therefore attracted attention for their potential to mitigate stress-related reproductive alterations. Coenzyme Q10 (CoQ10) is a lipid-soluble quinone involved in mitochondrial energy metabolism and is widely used as a dietary supplement. However, whether CoQ10 modulates female reproductive responses to repeated psychological stress remains unclear. Although water avoidance stress (WAS) is a well-established psychogenic stress model, its effects on female reproductive outcomes are still not fully defined. In this study, we examined how repeated WAS affects female reproductive outcomes and whether CoQ10 modifies these effects. Twenty-eight regularly cycling female rats were assigned to sham control, WAS, CoQ10, or WAS + CoQ10 groups. WAS was applied for 1 h/day for 10 days, and CoQ10 was administered orally at 100 mg/kg/day. Repeated WAS did not significantly alter sexual incentive motivation parameters, reproductive hormones, corticosterone, total antioxidant capacity (T-AOC), 8-hydroxy-deoxyguanosine (8-OHdG), or mast cell count under the present experimental conditions (all p > 0.05). However, WAS reduced male-directed active investigation time (p = 0.008) and male investigation preference ratio (p = 0.024), increased absolute ovarian and adrenal gland weights (p = 0.035 and p = 0.016, respectively), reduced primordial follicle number (p = 0.030), decreased germinative epithelium thickness (p = 0.017), lowered VEGF histoscore (p = 0.033) regardless of CoQ10 treatment, and reduced corpus luteum angiogenesis in animals not receiving CoQ10 (p = 0.030). CoQ10 reduced total investigation time toward the male (p = 0.032), male investigation preference ratio (p = 0.037), 17-β estradiol (E2) (p = 0.003), testosterone (p = 0.021), and germinative epithelium thickness (p < 0.001) regardless of WAS exposure. CoQ10 also decreased kisspeptin-1 levels under non-stressed conditions (p = 0.010), while increasing corpus luteum angiogenesis under stress conditions (p = 0.003). Overall, repeated WAS produced selective behavioral and ovarian alterations rather than broad reproductive dysfunction. CoQ10 was not associated with a broadly protective or uniformly beneficial profile in this model, and its endocrine, behavioral, and ovarian effects should be interpreted with caution. Full article

Background/Objectives: Neurodegenerative diseases such as Alzheimer’s disease (AD) and Parkinson’s disease (PD) represent a growing public health concern. Both disorders are driven by mitochondrial dysfunction, oxidative stress, impaired autophagy, neuroinflammation, and neuronal loss. Single-target therapeutics have failed to halt disease progression, highlighting the need for multi-target interventions that address the complex and interconnected nature of neurodegeneration. Natural health products (NHPs) such as curcumin (CUR), coenzyme-Q10 (CoQ10), and Ashwagandha (ASH) possess antioxidant, anti-inflammatory, neuroprotective, and neurotrophic properties that may collectively address this complex pathology. However, poor bioavailability and hydrophobicity have limited clinical translations. Novel formulations, including nanomicellar Ubisol-Q10 (UQ) and water-solubilized ASH (PTS-ASH), have demonstrated enhanced metabolic uptake and neuroprotective efficacy in preclinical models. Moreover, co-administered NHPs, such as CUR + CoQ10 and CoQ10 + ASH, may provide further benefits by diversified targeting of disease pathways. Methods: This review presents an integrative interpretation of a combined UQ + ASH “tonic” in transgenic AD and paraquat-induced PD animal models using previously published qualitative immunohistochemical and functional results. This report constructs a proposed mechanistic model illustrating how these compounds may interact across multiple stages of disease AD and PD progression. Results: Based on comprehensive interpretation of the previous published reports, consistent trends suggest UQ stabilizes mitochondrial energetics and suppresses oxidative damage upstream, whereas ASH promotes downstream repair and synaptic modulation. Combined administration remained as providing balanced neuroprotective and functional outcomes. Conclusions: These interpretations of published reports and proposed mechanistic models aim to improve the translation and support the therapeutic potential of multi-component natural interventions for neurodegenerative diseases and highlight the importance of bioavailability-enhancing formulations in future preclinical and clinical research. Full article

Cinnamomum camphora seed kernels are a potentially valuable fatty oil resource; however, their lipid composition and dynamic changes during development remain poorly understood. In this study, morphological and anatomical observations combined with liquid chromatography–tandem mass spectrometry (LC-MS/MS)-based lipidomics were used to investigate lipid accumulation patterns in C. camphora seed kernels across five developmental stages. The results showed that seed development followed a distinctive pattern in which morphological maturation preceded physiological maturity. A total of 627 lipid molecules were identified and classified into 27 subclasses and 5 major classes. Among them, glycerolipids (GLs) and glycerophospholipids (GPs) were the dominant lipid classes, with triacylglycerols (TGs) representing the principal storage lipids. Approximately 84.2% of the detected lipids were unsaturated, indicating a highly unsaturated lipid profile. The fatty acid composition was enriched in medium-chain fatty acids (MCFAs), especially decanoic acid and lauric acid, suggesting that C. camphora seed kernel oil possesses distinctive compositional characteristics compared with conventional fatty oils. In addition, coenzyme Q (CoQ) showed relatively high abundance and dynamic accumulation during seed development. Differential lipid analysis further revealed that lipid remodelling occurred mainly during the early developmental stages and was significantly associated with glycerolipid and glycerophospholipid metabolism. Diacylglycerols (DGs), phosphatidylcholines (PCs), and phosphatidylethanolamines (PEs) decreased during early development, whereas TGs accumulated continuously from the middle stage onwards. Overall, this study provides a systematic characterisation of lipid composition and developmental dynamics in C. camphora seed kernels and offers a theoretical basis for their future utilisation as a novel functional fatty oil resource. Full article

This study evaluated the effects of dietary coenzyme Q10 (CoQ10) supplementation on growth performance, slaughter performance, meat quality, antioxidant capacity, serum profiles, and intestinal morphology in Minxinan black rabbits. A total of 250 rabbits were allocated to five dietary treatments containing 0, 30, 60, 120, or 240 mg/kg CoQ10 for 14 weeks after a 1-week adaptation period. Results indicated that supplementation with 60 mg/kg CoQ10 resulted in the highest final body weight (2.83 kg) and average daily gain (29.54 g/day), with a significantly reduced feed-to-gain ratio and mortality rate compared to the control group. Regarding slaughter performance, the 60 mg/kg group significantly reduced the abdominal fat rate. In terms of meat quality, the 60 and 120 mg/kg groups showed significantly reduced drip loss and shear force, while meat lightness (L*) increased in all supplemented groups. Cooking loss was significantly reduced in the 60 mg/kg group. Antioxidant capacity in cardiac muscle and longissimus thoracis et lumborum (LTL) muscle was enhanced, particularly at 60 mg/kg, with significantly elevated activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and total antioxidant capacity (T-AOC), alongside reduced malondialdehyde (MDA) content. Furthermore, the 60 mg/kg group increased LTL muscle polyunsaturated fatty acid (PUFA) content, elevated serum levels of triiodothyronine (T3), growth hormone (GH), and insulin-like growth factor-1 (IGF-1), enhanced immunoglobulin concentrations, and improved intestinal morphology. In conclusion, dietary supplementation with 60 mg/kg CoQ10 improved growth performance, carcass leanness, PUFA content, and antioxidant status in broiler rabbits. Full article

Statins are commonly used cholesterol-lowering drugs, but their effects on astrocyte oxidative metabolism are poorly understood. To investigate this, rat astrocytes were exposed to 200 nM atorvastatin or simvastatin for 6 days and then assessed for changes in coenzyme Q (CoQ) homeostasis, mitochondrial function, and energy metabolism. Both statins comparably decreased cellular CoQ9 and CoQ10 levels (~35%), with greater losses of their reduced antioxidant forms (60–75%). Lower intracellular and mitochondrial levels of reactive oxygen species (ROS) were accompanied by the upregulation of nuclear factor erythroid 2-related factor 2 (NRF2)-dependent antioxidant pathways (superoxide dismutase 1 and glutathione reductase) and metabolic stress response factors, including hypoxia-inducible factor 1-alpha (HIF1α) and brain-derived neurotrophic factor (BDNF). Both statins promoted glycolytic reprogramming, mitochondrial fission, and biogenesis while impairing oxidative phosphorylation, as evidenced by reduced ATP-linked respiration, increased proton leak, and lower ATP levels. These findings suggest that statin-treated astrocytes adapt by prioritizing redox homeostasis over ATP production. CoQ10 supplementation increased cellular CoQ10 levels and restored ATP levels without further decreasing ROS, suggesting that its primary benefit is bioenergetic support, not additional antioxidant protection. Overall, statin-induced CoQ deficiency induces adaptive metabolic remodeling of astrocytes, while CoQ10 supplementation may help maintain energy metabolism under these conditions. Full article

Primary mitochondrial diseases (PMD) are rare disorders with limited therapeutic options. Coenzyme Q10 (CoQ10) supplementation is widely used, although formulation differences can affect absorption and efficacy. This open-label pilot feasibility trial evaluated a food for special medical purposes (FSMP) containing high-dose CoQ10 (250 mg per capsule) in patients with PMD. Ten patients (mean age: 55.5 ± 8.6 years) were enrolled. Serum/plasma biomarkers, including CoQ10, fibroblast growth factor 21 (FGF21), growth differentiation factor 15 (GDF15), ferric-reducing antioxidant power (FRAP), total sulfhydryl groups (t-SH), and advanced oxidation protein products (AOPP), were assessed at baseline (T0, after ≥30 days of conventional ubidecarenone) and after 30 days of FSMP administration (T1). Fatigue severity scale (FSS) and 5-times sit-to-stand test (5xSST) were evaluated at both timepoints. FSMP was administered at 250 or 500 mg/day. Twenty sex- and age-matched healthy controls were included for CoQ10 comparison. Absolute CoQ10 concentrations remained stable overall at T1, with all patients maintaining levels above 390 ng/mL (100% vs. 60% at T0), although concentrations remained lower than in healthy controls (p < 0.01). Dose-normalized CoQ10 exposure was significantly higher with FSMP versus conventional ubidecarenone (p < 0.001, Cohen’s d = 7.31). FGF21, GDF15, AOPP, and t-SH remained unchanged, whereas FRAP increased at T1 (p < 0.01). No significant changes were observed in 5xSST and FSS. Exploratory analyses indicated inter-individual variability in functional responses. FSMP was associated with higher dose-normalized systemic CoQ10 exposure, more consistent circulating CoQ10, and increased FRAP levels. Its simplified dosing regimen may support long-term adherence. Larger studies are warranted to validate these preliminary findings. Full article

Background/Objectives: L-carnitine and Coenzyme Q₁₀ (CoQ₁₀) are widely used in health and sports supplementation settings to improve energy metabolism, reduce fatigue, and support recovery. Although generally perceived as safe, their safety profiles are mainly based on pre-marketing studies and selected clinical populations, while real-world pharmacovigilance evidence remains limited. This study aimed to evaluate and compare the adverse drug reaction (ADR) reporting patterns associated with L-carnitine and CoQ10 using the EudraVigilance database. Methods: A retrospective pharmacovigilance analysis was conducted using spontaneous individual case safety reports (ICSRs) retrieved from the EudraVigilance database. ADRs associated with L-carnitine and CoQ₁₀ were analyzed and compared at the System Organ Class (SOC) level. Disproportionality analyses were performed using the reporting odds ratio (ROR) and proportional reporting ratio (PRR). Results: A total of 257 ICSRs for L-carnitine and 271 for CoQ10 were identified. Serious cases accounted for 34.2% of L-carnitine reports and 74.5% of CoQ₁₀ reports. For L-carnitine, the most frequently reported SOC categories were gastrointestinal disorders, skin and subcutaneous tissue disorders, general disorders and administration site conditions, and nervous system disorders. For CoQ₁₀, the most commonly reported SOC categories were general disorders and administration site conditions, nervous system disorders, investigations, and gastrointestinal disorders. Comparative disproportionality analysis showed higher reporting frequencies for CoQ₁₀ in blood and lymphatic system disorders (ROR 3.04; PRR 2.99), musculoskeletal and connective tissue disorders (ROR 2.63; PRR 2.52). Conclusions: Real-world pharmacovigilance data suggest partially different ADR reporting patterns for L-carnitine and CoQ₁₀ compared with those described in pre-marketing studies. CoQ₁₀ was associated with a higher proportion of serious reports and greater disproportionality signals for selected SOC categories; however, these findings should be interpreted cautiously, as reporting patterns may be influenced by reporting bias, comorbidities, concomitant therapies, and differences in the populations using these compounds. Continuous pharmacovigilance monitoring and periodic reassessment of their benefit–risk profile remain essential given their widespread use in health and sports supplementation settings. Full article

Cyclophosphamide (CTX)-induced premature ovarian failure (POF) is characterized by disruption of the follicular microenvironment, granulosa-cell loss, endocrine imbalance, and oxidative-inflammatory injury. Here, we evaluated two multi-bioactive formulations developed to enhance ovarian stress resilience: a base formulation containing coenzyme Q10, calcium L-5-methyltetrahydrofolate, and Vitex agnus-castus extract (Base), and a urolithin A-enriched formulation (Base + U). Using a CTX-induced female C57BL/6 mouse model, we integrated phenotypic, histological, endocrine, oxidative-inflammatory, and transcriptional readouts to assess efficacy and mechanistic consistency. CTX markedly reduced ovarian index, disrupted estrous cyclicity, shifted follicle development toward atresia, increased granulosa-cell apoptosis, and caused endocrine dysregulation, including decreased anti-Müllerian hormone and estradiol and increased GnRH, FSH, and LH. CoQ10, Base, and Base + U each partially alleviated these abnormalities, improving ovarian index and coat condition, showing a trend toward improved follicular distribution, and normalizing hormone profiles. CTX also induced an ovarian oxidative-inflammatory shift, as reflected by decreased GSH-Px, increased MDA, and elevated IL-1β, IL-6, and TNF-α, all of which were attenuated by the interventions. Notably, Base + U more effectively reduced lipid peroxidation and TNF-α than Base alone. Consistently, ovarian transcripts related to follicle responsiveness and steroid regulation, including Fshr, Esr1, and Hsd17b2, were restored, whereas hypothalamic qRT-PCR analysis did not reveal robust transcriptional alterations within the intervention window. These findings suggest that the urolithin A-enhanced formulation partially alleviates CTX-induced ovarian dysfunction by suppressing oxidative-inflammatory stress and preserving granulosa-cell and follicle fate. Full article

Cryopreservation of gametes is crucial for conserving genetic diversity in livestock and endangered species, but the process can significantly impair sperm quality due to oxidative stress. Our aim was to evaluate the impacts of coenzyme Q10 (CoQ10) supplementation on the in vitro quality of cooled and cryopreserved goat semen. Semen samples collected from six mature Saanen bucks were pooled then diluted with AndroMed^® semen extender to a final concentration of 800 × 10⁶ sperm/mL. Diluted semen was supplemented with 0, 1, 2, 5, 10, and 20 µM CoQ10. Extended semen was either cooled at 4 °C for 72 h or cryopreserved using a Styrofoam box in which the straws were arranged on the freezing rack and placed 4 cm over the liquid nitrogen (LN₂) for 10 min then stored in a LN₂ tank for one-week before being thawed at 37 °C for 30 sec. Sperm quality, including total and progressive motility, sperm kinematics, live sperm %, and sperm membrane integrity, was assessed at 0 h (fresh semen), and 24, 48, and 72 h post-cooling. For post-thaw sperm, we evaluated the same parameters plus acrosome integrity, mitochondrial activity, lipid peroxidation, and sperm ultrastructural changes using scanning electron microscopy (SEM). The pooled semen sample was considered the experimental unit for all treatments. Cooled semen data were analyzed using a General Linear Model (GLM) with univariate analysis, followed by Tukey’s test for multiple comparisons. In contrast, data from frozen–thawed semen were analyzed using one-way analysis of variance (ANOVA) followed by Tukey’s test. CoQ10 supplementation at 10 and 20 µM significantly (p < 0.05) improved sperm motility, viability, and membrane integrity in cooled and frozen–thawed semen in comparison with the control group (0 µM CoQ10). Moreover, the same concentrations significantly (p < 0.05) enhanced acrosome integrity, mitochondrial activity, and reduced the percentages of sperm with lipid peroxidation in frozen–thawed semen. Furthermore, 10 and 20 µM CoQ10 significantly mitigated the ultrastructural defects in frozen–thawed spermatozoa. In conclusion, CoQ10 supplementation during the cooling and cryopreservation of dairy goat semen significantly improved sperm quality. Among the tested concentrations, 10 and 20 µM exhibited the most favorable outcomes. Full article

Background: Coenzyme Q₁₀ and Alpha-lipoic acid are two essential antioxidants involved in numerous physiological processes, including cellular energy production and the mitigation of oxidative stress. Their accurate quantification is critical for understanding their biological roles and therapeutic potential. Herein, an RPLC-MS/MS method for the rapid and simultaneous determination of ubiquinone-10 (CoQ₁₀), the reduced form ubiquinol-10 (CoQ₁₀H₂), and Alpha-lipoic acid (ALA) in human serum was developed and validated. Methods: Chromatographic separation was performed on a Waters ACQUITY UPLC HSS T3 column (2.1 mm × 150 mm, i.d. 1.7 μm). Detection was performed on a SCIEX Triple Quad 6500+ system, applying multiple reaction monitoring (MRM). Single-phase protein precipitation was selected as the sample preparation protocol, providing satisfactory recovery for the analytes. Results: The method was linear over the concentration of 53.8–613 ng/mL for CoQ₁₀H₂, 23.1–263 ng/mL for CoQ₁₀ and 7.7–87.6 ng/mL for ALA. Intra- and inter-day accuracy was found to be between 81.8 and 109% and 84.4 to 106%, respectively, for all analytes, while intra- and inter-day precision was found to vary from 0.8% to 9.9% %RSD and 2.0% to 7.7% %RSD, respectively. A limit of quantitation (LOQ) of 4.2 ng/mL was found for CoQ₁₀H₂, 1.7 ng/mL for CoQ₁₀ and 0.7 ng/mL for ALA. Conclusions: The developed LC-MS/MS method enables rapid, sensitive and simultaneous quantification of CoQ₁₀H₂, CoQ_10, and ALA in human serum with satisfactory accuracy, precision and sensitivity. The method is suitable for bioanalytical applications and was successfully applied to the analysis of 10 real samples obtained from healthy volunteers. Full article

Oxidative stress and redox imbalance are central features of both age-related neurodegenerative disorders and the persistent neurological sequelae of coronavirus disease 2019. Increasing evidence suggests that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection disrupts neuronal redox homeostasis via mitochondrial dysfunction, iron dysregulation, inflammatory signaling, and the depletion of pyridine nucleotide pools. In that context, ferroptosis provides a unifying mechanistic framework linking lipid peroxidation to progressive neuronal injury. This review proposes that neuronal vulnerability might depend not only on the oxidative burden itself but also on the failure of membrane-localized antioxidant defenses. Particular emphasis is placed on the plasma membrane redox system (PMRS), a membrane-associated quinone-reducing network that can support coenzyme Q redox cycling and constrain lipid radical propagation at the plasma membrane. Unlike canonical ferroptosis defense systems that rely predominantly on NADPH, components of the PMRS, particularly cytochrome b5 reductase, can also use NADH, conferring partial metabolic flexibility in conditions of redox stress. We further discuss how SARS-CoV-2-induced NAD⁺ depletion might progressively destabilize this membrane-proximal defense architecture, potentially lowering the ferroptotic threshold of vulnerable neurons. Finally, we outline therapeutic strategies that might reinforce PMRS-dependent membrane redox control through NRF2 activation, NAD⁺ restoration, coenzyme Q-centered interventions, and modulation of iron-catalyzed lipid oxidation. Full article

Coenzyme Q10 (CoQ10), a natural antioxidant produced by the human body, has strong anti-inflammatory properties, reduces oxidative stress, and improves mitochondrial function. It is also known for its strong neuroprotective effects. With age, endogenously produced CoQ10 levels decline, contributing to the development of chronic diseases, including eye disorders. Irreversible ocular diseases that result in blindness present a significant challenge in contemporary medicine, as no fully effective cure exists; current treatments primarily aim to decelerate disease progression, manage symptoms, and preserve residual vision. Our study reviews research on the use of CoQ10 in eye diseases like age-related macular degeneration (AMD), retinitis pigmentosa (RP), and glaucoma, which can cause permanent vision loss and are linked to oxidative stress and mitochondrial dysfunction. This article explores whether CoQ10 can be a safe and effective addition to treatment for these conditions. We also outline directions for future research and explain how CoQ10 functions in the studies discussed in this review. Full article

Primary coenzyme Q10 (CoQ10) deficiency results from mutations in genes involved in the CoQ10 biosynthetic pathway. In humans, at least 10 genes (PDSS1, PDSS2 to COQ10) are required for the biosynthesis of functional CoQ10, a mutation in any one of which can result in a deficit in CoQ10 status and present as primary CoQ10 deficiency. Furthermore, the genes NDUFA9 and HPDL, whilst not part of the PDSS1, PDSS2 to COQ10 gene sequence, have also been shown to have a crucial role in CoQ10 biosynthesis. A major problem in treating primary CoQ10 deficiencies is the poor bioavailability of supplemental CoQ10, both in terms of lack of absorption from the digestive tract and inability to cross the human blood–brain barrier. Bypass strategies aim to circumvent this problem by using more bioavailable precursor analogues that can enter the cell and be incorporated into the CoQ10 synthesis pathway downstream of the affected enzyme, examples being 4-hydroxybenzoic acid, 2,4-dihydroxybenzoic acid or vanillic acid, which, in contrast to CoQ10, are small, water-soluble molecules. In this article, we have, therefore, reviewed potential bypass mechanisms for primary CoQ10 deficiencies, PDSS1, PDSS2 to COQ10, together with NDUFA9 and HPDL, using such precursors. Most of the published data relating to the bypass therapy of primary CoQ10 deficiency is derived from cell lines or animal models, and few human studies have so far been undertaken. In addition, further research is required to investigate the potential mechanisms by which bypass compounds such as 4-HB may access the human blood–brain barrier (BBB), for example, using in vitro co-culture BBB model systems incorporating CoQ10-deficient neurons. Overall, the objective of this article is, therefore, to systematically review the available data for each of the primary CoQ10 deficiencies, PDSS1, PDSS2 to COQ10 together with NDUFA9 and HPDL, in particular to identify the clinical potential of such studies. Full article

Congenital heart diseases (CHDs) are characterized by profound metabolic remodeling of mitochondrial pathways. However, data regarding mitochondrial respiration, oxidative phosphorylation (OXPHOS), and fatty acid oxidation (FAO) in patients with Ebstein anomaly (EA) are currently unavailable. This study evaluated 14 EA patients and 18 healthy volunteers. In accordance with the 2020 ESC guidelines, patients were stratified into two cohorts: EA-0 (patients currently without an indication for intervention) and EA-1 (patients meeting Class Ia or IIb indications for surgical intervention). Platelet OXPHOS and FAO parameters were determined simultaneously via high-resolution respirometry. CI-linked LEAK respiration (substrates: pyruvate and malate) and FAO-linked LEAK respiration (substrates: octanoylcarnitine and malate) were significantly elevated in EA patients. Furthemore, the EA-1 group showed significantly lower coenzyme Q₁₀ (CoQ₁₀) and γ-tocopherol levels than EA-0. Differences in the measured parameters between groups suggest a state of myocardial adaptation and transient metabolic reprogramming in EA-0 patients, whereas in EA-1 patients, a significant change in mitochondrial metabolism and bioenergetics was found. We hypothesize that increased platelet LEAK mitochondrial respiration and CoQ₁₀ deficiency could be key signals of mitochondrial reprogramming and serve as potential biomarkers for right ventricular dysfunction. The analysis of platelet mitochondrial bioenergetics represents a novel area of translational mitochondrial cardiology, contributing to personalized diagnostics, risk stratification and optimal surgical timing in EA patients. Full article

This study aimed to evaluate the impact of coenzyme Q10 (CoQ10) supplementation during in vitro maturation (IVM) and/or vitrification of immature dromedary camel oocytes on their subsequent in vitro developmental competence. Additionally, total antioxidant capacity (TAC) and malondialdehyde (MDA) concentrations were assessed in the IVM spent medium. In experiment 1, cumulus–oocyte complexes (COCs, n = 808) collected from slaughtered dromedary camel ovaries were cultured in IVM media supplemented with either 0, 25, 50, or 100 μM CoQ10 for 36 h. Matured oocytes were then fertilized in vitro with epididymal camel spermatozoa. Eighteen hours post-insemination (pi), presumptive zygotes were cultured in vitro for 7 days. In experiment 2, a total of 875 COCs were randomly allocated to one of four experimental groups, namely (a) Vit−/IVM− (control) group, where COCs were vitrified in vitrification solution (VS; 25% DMSO + 25% EG) and matured in IVM media without CoQ10 supplementation; (b) Vit+/IVM− group, in which COCs were vitrified in a VS supplemented with 50 µM CoQ10 and matured in IVM media without CoQ10 supplementation; (c) Vit−/IVM+ group, where COCs were vitrified in VS without CoQ10 supplementation and matured in IVM media supplemented with 50 µM CoQ10; and (d) Vit+/IVM+ group, where COCs were vitrified in VS and matured in IVM media, both supplemented with 50 µM CoQ10. Following vitrification and warming, oocyte viability was evaluated morphologically and by trypan blue staining. Viable oocytes were then matured, fertilized, and cultured in vitro. In experiment 3, TAC and MDA concentrations in the IVM spent media were analyzed. Results showed that 50 µM CoQ10 supplementation to IVM media enhanced cumulus expansion, nuclear maturation, cleavage, and blastocyst rates (experiment 1). Adding 50 µM CoQ10 to the VS enhanced (p ≤ 0.05) oocyte viability compared to those vitrified in CoQ10-free media. Cumulus cell expansion and nuclear maturation rates were higher (p ≤ 0.05) in Vit−/IVM+ than in Vit+/IVM+ and Vit−/IVM− groups. Furthermore, cleavage and blastocyst rates were the highest (p ≤ 0.05) in Vit−/IVM+ group (experiment 2). The concentrations of TCA were higher, and the concentrations of MDA were lower (p ≤ 0.05) in Vit−/IVM+ than in other groups (experiment 3). In conclusion, supplementation of CoQ10 in the maturation medium of vitrified–warmed immature dromedary camel oocytes may enhance their in vitro developmental competence. Full article